As a result, the effect of EA was similar to pharmacologic blockade of IDO1, 1-MT, abrogating the IDO activity and decreasing the content of KYN and QA to protect from inflammation-induced IDO-dependent neurotoxic kynurenine metabolism, which was a pathogenic factor for inflammation-induced depressive disorders and a potential novel target for the treatment of these disorders (Heisler and O’connor, 2015). Here, IDO1 is linked to depressive disorder.